By K. Osmund. University of New Mexico.

Occasionally generic januvia 100 mg line diabetes type 2 feet, the patient may complain of nasal obstruction buy 100mg januvia amex diabetes insipidus juvenile, discomfort buy januvia 100 mg on line diabetes symptoms hungry all the time, or difficulties in wearing dentures. Differential diagnosis Soft-tissue abscess, tooth abscess, mucocele, radicular cyst, salivary gland neoplasms, mesenchymal neoplasms. Palatine Papilla Cyst Definition Palatine papilla cyst is a variety of the nasopalatine cyst. Clinical features It appears as a slow-growing soft swelling of the palatine papilla, covered with normal mucosa (Fig. The cyst, after mechanical irritation, may be inflamed and becomes painful due to local infection. Differential diagnosis Tooth and periodontal abscesses, mechanical trauma of the palatine papilla, fibroma, lipoma. Usage subject to terms and conditions of license Laskaris, Pocket Atlas of Oral Diseases © 2006 Thieme All rights reserved. Usage subject to terms and conditions of license 313 10 Bone Swellings Bone swellings are lesions that characteristically present as asymptom- atic hard lumps, covered by normal epithelium. Developmental disor- ders, benign and malignant tumors are included in this group of lesions. O Torus mandibularis O Chondrosarcoma O Torus palatinus O Burkitt lymphoma O Multiple exostoses O Multiple myeloma O Osteoma O Paget disease O Osteosarcoma O Odontogenic tumors Laskaris, Pocket Atlas of Oral Diseases © 2006 Thieme All rights reserved. Usage subject to terms and conditions of license 314 Bone Swellings Torus Mandibularis Definition and etiology Torus mandibularis is a developmental mal- formation of unknown etiology. Clinical features It presents as an asymptomatic bony swelling, cov- ered by normal mucosa. Characteristically, the lesions appear bilaterally on the lingual surface of the mandible, usually in the area adjacent to the bicuspids (Fig. Torus Palatinus Definition and etiology Torus palatinus is a developmental malforma- tion of unknown etiology. Clinical features It presents as a slow-growing, nodular, lobular or spindled, asymptomatic bony swelling covered by normal mucosa. Char- acteristically, the lesion appears along the midline of the hard palate (Fig. It occurs more often in women, and usually appears during the third decade of life. Usage subject to terms and conditions of license 316 Bone Swellings Multiple Exostoses Multiple exostoses (see p. Osteoma Definition Osteoma is a benign neoplasm that consists of mature compact or cancellous bone. Clinical features It presents as an asymptomatic, slow-growing bony swelling of the jaws. Usage subject to terms and conditions of license 318 Bone Swellings Osteosarcoma Definition Osteosarcoma is the most common primary malignant neo- plasmof bone. Clinical features The jaws are affected in 6–7% of cases, and usually during the third decade of life. Clinically, the lesion presents as a rapidly growing hard swelling that progressively produces facial deformity (Fig. Differential diagnosis Chondrosarcoma, Ewing sarcoma, metastatic tumors, odontogenic tumors and cysts, giant-cell tumor. Clinically, it appears as a painless hard swelling that progressively enlarges, causing extensive bone destruction with pain and loosening of the teeth. Burkitt Lymphoma Definition Burkitt lymphoma is a high-grade malignant B-lymphocyte lymphoma. Clinical features The malignancy is prevalent in central Africa (the endemic form), and usually affects children 2–12 years of age. The jaws are the most common site of Laskaris, Pocket Atlas of Oral Diseases © 2006 Thieme All rights reserved. Usage subject to terms and conditions of license 320 Bone Swellings lymphoma (60–70%). Clinically, it presents as a rapidly growing hard swelling that causes bone destruction, tooth loss, and facial deformity (Fig. Pain, paresthesia and large ulcerating or nonulcerating masses may also be seen (Figs. Differential diagnosis Central giant-cell granuloma, ossifying fibroma, other non-Hodgkin lymphomas, and odontogenic tumors. Usage subject to terms and conditions of license 322 Bone Swellings Multiple Myeloma Definition Multiple myeloma is a relatively rare malignant plasma-cell disorder. Clinical features The malignancy is more common in men over 50 years of age, and the jaws are affected in about 30% of cases. Clinically, it presents with bone swelling, tooth mobility, pain, and paresthesia. A painless soft swelling, usually on the alveolar mucosa and gingiva, may develop as part of the overall disease spectrum(Fig. Laboratory tests Bone-marrow biopsy, radiography, serum and urine protein electrophoresis. Differential diagnosis Plasmacytoma, non-Hodgkin lymphoma, Ewing sarcoma, leukemia, Langerhans cell histiocytosis. Paget Disease Definition Paget disease, or osteitis deformans, is a chronic, relatively common disorder characterized by uncoordinated bone resorption and deposition. Clinical features Clinically, the signs and symptoms develop gradually and are characterized by bone pain, headache, deafness, visual disorders, dizziness, and progressive bone enlargement. Progressive expansion of the maxilla and the mandible lead to symmetrical thickening of the alveolar ridges (Fig. Edentulous patients may complain that their dentures do not fit due to alveolar enlargement (Fig. Delayed wound healing, bleeding, and osteomyelitis after tooth extraction may occur. Two major forms of the disease are recognized: (a) the monostotic, and (b) the polyostotic. Usage subject to terms and conditions of license 324 Bone Swellings The clinical diagnosis should be confirmed by a histopathological and radiographic examination. Elevations of serum alkaline phosphatase and urinary hydroxyproline levels are common findings. Differential diagnosis Fibrous dysplasia, osteosarcoma, multiple exos- toses, fibro-osseous lesions.

Acute Schmorl’s node may cause pain and the surrounding ver- The most obvious changes in degenerative diseases of the tebral bone marrow may show diffuse marrow edema [9] 100 mg januvia with visa diabetes burnout definition. The outgrowths are called pain januvia 100mg on-line diabetes mellitus without complication type 2, it is not only important to report the morphology effective 100mg januvia diabetes type 2 quinoa, lo- osteophytes or spondylosis deformans. Osteophytes arise cation, and size of the disk abnormality, but also to describe in the setting of disk degeneration when Sharpey fibers the relationship between the disk and the nerve root. According to this classification sys- ly, particularly in the lateral recesses of the spinal canal tem, the relationship between the disk and the nerve root is or in the intervertebral foramen. Although the grading joints are true synovial joints, with hyaline articular car- system is primarily based on the assessment of axial images, tilage, a synovial membrane and a joint capsule. Facet sagittal images are also useful, in particular to detect com- joint osteoarthritis does not differ from degenerative promise of the nerve root within the neuroforamina. There is commonly tears (synonym: anular fissure) are separations between a proliferative response involving the formation of osteo- anular fibers, avulsion of fibers from their vertebral-body phytes and sclerosis of subchondral bone. In addition, insertions, or breaks through fibers involving one or subchondral cysts and synovial inflammation may be pre- many layers of the anular lamellae. Other forms of ac- a b quired central stenosis include iatrogenic stenosis, trau- matic stenosis, and miscellaneous causes of stenosis (e. Cervical Spinal Stenosis In the cervical spine, central canal stenosis is caused by osteophytosis and ligamentous thickening. In the cervical spine, the width of the spinal canal is often quan- titatively assessed on radiographs since such measure- ments are predictive for the presence of spinal canal stenosis. In addition, anterolisthesis at the same level is noted and the anteroposterior diameter of the vertebral body. If the area of the dural sac is below 75 mm2, the likelihood of a stenosis is high. The lateral recess is bordered posteriorly by the su- perior articular facet, laterally by the pedicle and anteri- orly by the vertebral body and disk. Lumbar lateral recess stenosis occurs when a hypertrophic superior facet en- croaches on the recess, often in combination with nar- rowing due to a bulging disk and osteophyte. Foraminal stenosis occurs when a hypertrophic facet, vertebral-body osteophyte, or bulging disk narrows the neural foramen Fig. A 68-year-old woman with clinical symptoms of cervical and encroaches on the nerve roots. On conventional lateral radiographs the dis- Magnetic resonance imaging has extensively been used in tance between the posterior surface of the vertebral body the identification of abnormal conditions of the lumbar and the spinolaminar line can be measured. A spinal cord spine and has become the gold standard in evaluation of compression may be diagnosed if this distance is 10 mm spinal pathology. However, particularly in studying pa- or less, whereas if this distance is 13 mm or more then tients with low back pain, there is often a discrepancy be- spinal canal stenosis is unlikely. In addition, previous studies report- dural sac is reliable parameter for assessment of cervical ed a high rate of abnormal imaging findings in the lum- spine stenosis. A cross-sectional area of 60 mm2 has been bar spine of asymptomatic volunteers (Table 2) [15-22]. Since disk abnormalities, including disk bulging, disk Spinal canal stenosis may result in cervical myelopathy, protrusion and disk extrusion, are common in asympto- which presents as high signal intensity on T2-weighted matic volunteers, they cannot be used easily as parame- images (Fig. The pathophysiologic mechanisms that cause nerve- Myelography has for many years been the method of root symptoms are still not completely understood. For Currently, two concepts are discussed: mechanical nerve- clinical purposes, an anteroposterior diameter of the dur- root compression and chemically induced nerve-root in- al sac of 10 mm is indicative of absolute stenosis and 12 flammation caused by the nucleus pulposus [23]. A recent longitudinal study has shown that ligamentum flavum and intervertebral disk to the spinal type I endplate changes are dynamic lesions that either nerve roots in the lumbar spine. Based on these data, at a statistically significant level, that conversion from clinically relevant spinal canal and foraminal stenosis, as type 1 to type 2 is related to an improvement in the pa- well as the degree of nerve-root compression, may not be tient’s back pain [25]. Radiology 206(1):49-55 The clinical efficacy of magnetic resonance imaging in neu- 18. Radiology 169(1):93-97 racy of magnetic resonance imaging, work perception, and 4. Aviat Space Environ (2001) Magnetic resonance classification of lumbar interver- Med 67(9):849-853 tebral disc degeneration. J task Forces of the North American Spine Society, American Bone Joint Surg Am 72(3):403-408 Society of Spine Radiology, and American Society of 22. Resnick D, Niwayama G (1995) Degenerative disease of the cleus pulposus induces neurophysiologic and histologic spine. In: Resnick D (ed) Diagnosis of bone and joint disor- changes in porcine cauda equina nerve roots. Aprill C, Bogduk N (1992) High-intensity zone: a diagnostic Lumbar disc high-intensity zone. Correlation of magnetic res- sign of painful lumbar disc on magnetic resonance imaging. Most of the classic terms applied to osteomyelitis refer to chronic osteomyelitis, but the ability to make the diagnosis clinically at an ear- lier stage of disease is important. As we will see, the tibia of a child shows a dis- advanced imaging techniques play a role in early diag- crete radiolucent area in the nosis [2]. Extending su- periorly is a linear lucent tract that has not yet reached the cor- Features of Osteomyelitis tex. This linear tract is typical of Brodie’s abscess Acute Osteomyelitis The initial clinical presentation of acute osteomyelitis latent form of subacute or chronic infection is sclerosing will depend on the history and physical findings. The radiographic signs are usual- Radiography is often negative in the early stages of in- ly nonspecific. Treatment with antibiotics may be need to be biopsied in order to rule out a slow-growing needed before radiographs become positive. The lack of a clinical response may Chronic Osteomyelitis be an indication for biopsy in order to confirm the in- fecting organism or to rule out a tumor that is mimick- The body reacts to chronic infection in bone by destroy- ing osteomyelitis, such as Ewing’s sarcoma and lym- ing bone and producing new bone. Periosteal cloaking is the new bone surrounding an area Subacute Osteomyelitis of medullary infection in a long bone. A similar type of healing response in the periosteum in the case of fracture Brodie’s abscess is a term applied to one form of suba- is called callus. The radiographic signs are typical – a dead infected bone that has lost its blood supply. The the surrounding area is undergoing bone resorption sec- margins are usually sharply defined, indicating the slow ondary to the inflammatory response, the dead bone ap- progression of the infection.

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Isolation of organisms of the same phage type from stools or vomitus of 2 or more ill persons confirms the diagnosis discount januvia 100mg with mastercard managing your diabetes care. Recovery of large numbers of enterotoxin- producing staphylococci from stool or vomitus from a single person supports the diagnosis discount 100mg januvia otc diabetes type 1 cure june 2013. Phage typing and enterotoxin tests may help epidemiological investigations but are not routinely available or indicated; in outbreak settings purchase januvia 100 mg with amex diabetic diet hummus, pulsed field gel electrophoresis may be more useful in subtyping strains. Toxic agent—Several enterotoxins of Staphylococcus aureus, sta- ble at boiling temperature, even by thermal process. Staphylococci multiply in food and produce the toxins at levels of water activity too low for the growth of many competing bacteria. Occurrence—Widespread and relatively frequent; one of the prin- cipal acute food intoxications worldwide. Reservoir—Humans in most instances; occasionally cows with infected udders, as well as dogs and fowl. Toxin has also developed in inadequately cured ham and salami, and in unprocessed or inadequately processed cheese. When these foods remain at room tem- perature for several hours before being eaten, toxin-producing staphylo- cocci multiply and elaborate the heat-stable toxin. Organisms may be of human origin from purulent discharges of an infected finger or eye, abscesses, acneiform facial eruptions, nasopharyn- geal secretions or apparently normal skin; or of bovine origin, such as contaminated milk or milk products, especially cheese. Incubation period—Interval between eating food and onset of symptoms is 30 minutes to 8 hours, usually 2–4 hours. Preventive measures: 1) Educate food handlers about: (a) strict food hygiene, sani- tation and cleanliness of kitchens, proper temperature control, handwashing, cleaning of fingernails; (b) the dan- ger of working with exposed skin, nose or eye infections and uncovered wounds. If they are to be stored for more than 2 hours, keep perishable foods hot (above 60°C/140°F) or cold (below 7°C/45°F; best is below 4°C/39°F) in shallow con- tainers and covered. Control of patient, contacts and the immediate environment: 1) Report to local health authority: Obligatory report of out- breaks of suspected or confirmed cases in some countries, Class 4 (see Reporting). The prominent clinical features, coupled with an estimate of the incubation period, provide useful leads to the most probable causal agent. Collect specimens of feces and vomitus for laboratory examination; alert the laboratory to suspected causal agents. Conduct an epidemiological investigation including inter- views of ill and well persons to determine the association of illness with consumption of a given food. Compare attack rates for specific food items eaten and not eaten; the implicated food item(s) will usually have the greatest differ- ence in attack rates and most of the sick will remember having eaten the contaminated food. Look for possible sources of contamination and periods of inad- equate refrigeration and heating that would permit growth of staphylococci. Submit leftover suspected foods promptly for laboratory examination; failure to isolate staphylococci does not exclude the presence of the heat-resistant entero- toxin if the food has been heated. Antibiograms and/or phage typing of representative strains of enterotoxin producing staphylococci isolated from foods and food handlers and from patient vomitus or feces may be helpful. Disaster implications: A potential hazard in situations involv- ing mass feeding and lack of refrigeration facilities, including feeding during air travel. Identification—An intestinal disorder characterized by sudden onset of colic followed by diarrhea; nausea is common, vomiting and fever are usually absent. Generally a mild disease of short duration, 1 day or less, rarely fatal in healthy people. Outbreaks of severe disease with high case-fatality rates associated with a necrotizing enteritis have been docu- mented in postwar Germany and in Papua New Guinea (pigbel). When serotyping is possible, the same serotype is usually demonstrated in different specimens; serotyping is done routinely only in Japan and the United Kingdom. Occurrence—Widespread and relatively frequent in countries with cooking practices that favor multiplication of clostridia to high levels. Mode of transmission—Ingestion of food containing soil or feces and then held under conditions that permit multiplication of the organism. Almost all outbreaks are associated with inadequately heated or reheated meats, usually stews, meat pies, and gravies made of beef, turkey or chicken. Spores survive normal cooking temperatures, germinate and multiply during slow cooling, storage at ambient temperature, and/or inadequate rewarming. Outbreaks are usually traced to catering firms, restaurants, cafeterias and schools with inadequate cooling and refrigera- tion facilities for large-scale service. Illness results from the release of toxin by cells undergoing sporulation in the lower intestinal tract. Heavy bacterial contamination (more than 105organisms/gram of food) is usually required to produce toxin in the human intestine for clinical disease. Preventive measures: 1) Educate food handlers about the risks inherent in large-scale cooking, especially of meat dishes. Where possible, encour- age serving hot dishes (above 60°C/140°F) while still hot from initial cooking. Do not partially cook meat and poultry one day and reheat the next, unless it can be stored at a safe temperature. Large cuts of meat must be thoroughly cooked; for more rapid cooling of cooked foods, divide stews and similar dishes prepared in bulk into many shallow containers and place in a rapid chiller. Control of patient, contacts and the immediate environment, Epidemic measures and Disaster implica- tions: See Staphylococcal food intoxication (I, 9B, 9C and 9D). Identification—An intoxication characterized in some cases by sudden onset of nausea and vomiting, and in others by colic and diarrhea. In outbreak settings, diagnosis is confirmed through quantitative cul- tures on selective media to estimate the number of organisms present in the suspected food (generally more than 105to 106organisms per gram of the incriminated food are required). Isolation of organisms from the stool of 2 or more ill persons and not from stools of controls also confirms the diagnosis. Two enterotoxins have been identified: one (heat stable) causing vomiting, is produced in food when B. Reservoir—A ubiquitous organism in soil and environment, com- monly found at low levels in raw, dried and processed foods.

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The characteristic lesion buy discount januvia 100 mg diabetes in dogs insulin pills, caused by liberation of a specific cytotoxin cheap januvia 100mg with visa free diabetes test las vegas, is an asymmetrical adherent greyish white membrane with surrounding inflammation buy januvia 100mg fast delivery diabetic diet plan diabetic food list. The throat is moderately to severely sore in faucial or pharyngotonsillar diphtheria, with cervical lymph nodes somewhat enlarged and tender; in moderate to severe cases, there is marked swelling and oedema of the neck with extensive tracheal membranes that progress to airway obstruction. Nasal diphtheria can be mild and chronic with one-sided nasal discharge and excoriations. The toxin can cause myocarditis, with heart block and progressive congestive failure beginning about 1 week after onset. The lesions of cutaneous diphtheria are variable and may be indistinguishable from, or a component of, impetigo; peripheral effects of the toxin are usually not evident. Case-fatality rates of 5%–10% for noncutaneous diphtheria have changed little in 50 years. Diphtheria should be suspected in the differential diagnosis of bacterial (especially streptococcal) and viral pharyngitis, Vincent angina, infectious mononucleosis, oral syphilis and candidiasis. Presumptive diagnosis is based on observation of an asymmetrical, greyish white membrane, especially if it extends to the uvula and soft palate and is associated with tonsillitis, pharyngitis or cervical lymphade- nopathy, or a serosanguineous nasal discharge. If diphtheria is strongly suspected, specific treatment with antibiotics and antitoxin should be initiated while studies are pending and continued even in the face of a negative laboratory report. Infectious agent—Corynebacterium diphtheriae of gravis, mitis or intermedius biotype. Toxin production results when bacteria are infected by corynebacteriophage containing the diphtheria toxin gene tox. Nontoxigenic strains rarely produce local lesions; however, they have been increasingly associated with infective endocarditis. Occurrence—A disease of colder months in temperate zones, primarily involving nonimmunized children under 15; often found among adults in population groups whose immunization was neglected. In the tropics, seasonal trends are less distinct; inapparent, cutaneous and wound diphtheria cases are much more common. A massive outbreak of diphtheria began in the Russian Federation in 1990 and spread to all countries of the former Soviet Union and Mongolia. This epidemic declined after reaching a peak in 1995; it was responsible for more than 150 000 reported cases and 5000 deaths (1990–1997). In Ecuador, an outbreak of about 200 cases, half of whom were 15 or older, occurred in 1993–94. Mode of transmission—Contact with a patient or carrier; more rarely, contact with articles soiled with discharges from lesions of infected people. Period of communicability—Variable, until virulent bacilli have disappeared from discharges and lesions; usually 2 weeks or less, seldom more than 4 weeks. Susceptibility—Infants born to immune mothers have passive protection, which is usually lost before the 6th month. Disease or inapparent infection usually, but not always, induces lifelong immunity. Many of these older adults may have immunological memory and would be protected against disease after exposure. Antitoxic immunity protects against systemic disease but not against colonization in the nasopharynx. Preventive measures: 1) Educational measures are important: inform the public, particularly parents of young children, of the hazards of diphtheria and the need for active immunization. The first 3 doses are given at 4- to 8-week intervals beginning when the infant is 6 8 weeks; a fourth dose 6–12 months after the third dose. This schedule should not entail restarting immunizations because of delays in administering the scheduled doses. A fifth dose is given at 4–6 years prior to school entry; this dose is not necessary if the fourth dose was given after the fourth birthday. For a previously unimmu- nized individual, a primary series of 3 doses of adsorbed tetanus and diphtheria toxoids (Td) is advised, 2 doses at 4- to 8-week intervals and the third 6 months to 1 year after the second dose. Limited data from Sweden sug- gest that this regimen may not induce protective anti- body levels in most adults, and additional doses may be needed. Control of patient, contacts and the immediate environment: 1) Report to local health authority: Case report obligatory in most countries, Class 2 (see Reporting). Where culture is impractical, isolation may end after 14 days of appropriate antibiotherapy (see 9B7). Those who handle food or work with school children should be excluded from work or school until proven not to be carriers. Some erythromycin- resistant strains have been identified, but they are uncom- mon and not a public health problem. Newer macrolide antibiotics, including azythromycin and clarithromycin, do not offer any substantial advantage over erythromycin. Epidemic measures: 1) Immunize the largest possible proportion of the population group involved, especially infants and preschool children. In an epidemic involving adults, immunize groups that are most affected or at high risk. Repeat immunization proce- dures 1 month later to provide at least 2 doses to recipients. In areas with appropriate facilities, carry out a prompt field investigation of reported cases to verify the diagnosis and to determine the biotype and toxigenicity of C. Disaster implications: Outbreaks can occur when social or natural conditions lead to crowding of susceptible groups, especially infants and children. This frequently occurs when there are large-scale movements of susceptible populations. International measures: People travelling to or through countries where either faucial or cutaneous diphtheria is com- mon should receive primary immunization if necessary, or a booster dose of Td for those previously immunized. Identification—An intestinal tapeworm infection of long duration; symptoms commonly are trivial or absent. A few patients in whom the worms are attached to the jejunum rather than to the ileum develop vitamin B12 deficiency anaemia. Massive infections may be associated with diarrhea, obstruction of the bile duct or intestine, and toxic symptoms. Identification of eggs or segments (proglottids) of the worm in feces confirms the diagnosis. Occurrence—The disease occurs in lake regions in the northern hemisphere, and subarctic, temperate and tropical zones where eating raw or partly cooked freshwater fish is popular. In North America, endemic foci have been found among Eskimos in Alaska and Canada.

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